Reviewed by Cameron Wybrow
“In 1996, Pennsylvania’s own Michael J. Behe launched a frontal attack upon Darwinian evolution with the publication of Darwin’s Black Box. Behe, a mild-mannered molecular biologist at Lehigh University, argued politely but vigorously that the standard Darwinian explanation (random mutations plus natural selection) simply couldn’t explain the evolution of a number of significant structures and processes observed in living things. Intricate processes like human blood clotting, and intricate structures like the bacterial flagellum (which is built uncannily like an outboard motor) were “irreducibly complex” arrangements that couldn’t have arisen by a series of chance steps. They therefore must have been designed, by an intelligence of some kind. Behe’s book soon became the flagship of the movement known as intelligent design (ID).Behe’s presentation and subsequent defense of ID (including his testimony at the Dover trial in 2005) outraged much of the biological community. He was denounced by the self-styled defenders of science – biologists like Ken Miller and Jerry Coyne, and non-scientists like Michael Ruse and Barbara Forrest. They accused Behe (along with his allies in the ID movement) of recycling disproved arguments, of insolently refusing to genuflect before the Darwinian consensus, of misunderstanding the nature of scientific theory, and of trying to slip God (disguised as “the intelligent designer”) into public-school science classrooms. Intelligent design, if not nipped in the bud, would turn science classes into seminaries, set back modern medicine by denying the evolution of antibiotic resistance, and destroy confidence in science in general, relegating America to a backward technological status.There was some reasonable criticism. Behe said that the bacterial flagellum could have been created only by multiple coordinated genetic changes, and that such coordination was beyond the power of random mutation. Miller argued that, given enough time, random mutations could accumulate, producing a flagellum by stages. Behe’s purely qualitative argument couldn’t disprove this possibility; without hard numbers, how did he know what random mutation could or couldn’t accomplish?Behe’s new book, The Edge of Evolution, provides some hard numbers, coupled with an ingenious argument. The key to determining the exact powers of Darwinian evolution, says Behe, lies with fast-reproducing microbes. Some, such as malaria, HIV, and E. coli, reproduce so quickly that within a few decades, or at most a few millennia, they generate as many mutations as a larger, slower-breeding animal would in millions of years. By observing how far these creatures have evolved in recent times, we can estimate the creative limits of random mutation.

In the case of malaria, the creative limits appear quite low. Over the last few thousand years, several thousand billion billion malarial cells have been unable to develop an evolutionary response to the sickle-cell mutation, which protects its human bearers from malaria. On the other hand, malaria has proved able to develop Darwinian resistance to the antibiotic chloroquine. This resistance is based upon two simultaneous mutations affecting a malarial protein. Yet this rare double mutation has occurred fewer than 10 times since chloroquine was introduced 50 years ago, during which time a hundred billion billion malarial cells have been born. If this indicates the typical rate of occurrence of double mutations, then the Darwinian transformation of our pre-chimp ancestor into homo sapiens, which would have required at least some double mutations, would have taken at least a thousand trillion years, a time span greater than the age of the universe.

Drawing upon parallel mutation studies of HIV and E. coli for confirmation, Behe concludes that random mutations cannot explain the origin of most of the complex structures in living things. He concedes that Darwinian processes can make new species, but argues that they are incompetent to generate new kingdoms, phyla, or classes. The creative limit, the “edge of evolution,” lies somewhere between the level of species and the level of class. Darwinian processes can account for the difference between a dog and a wolf, maybe even a dog and a bear, but not the difference between a lizard and a bird. Something other than random mutation must have produced such differences; for Behe, the “something” is intelligent design.

The response to Behe has been predictable. The editors of the major print media have assigned known enemies of ID to trash the book – Richard Dawkins for the New York Times; Coyne for the New Republic; Miller for Nature; Ruse for Toronto’s Globe & Mail. A large part of each review is ad hominem, concerned with Behe’s alleged religious agenda, his minority status among biologists, and other irrelevant matters. In Dawkins’ review, the science is barely touched, and it’s not clear from Ruse’s review that he has even opened the cover of the book. Behe deserves better. The Edge of Evolution makes a serious, quantitative argument about the limits of Darwinian evolution. Evolutionary biology cannot honestly ignore it.”

Cameron Wybrow is a freelance writer with a doctorate from McMaster University. He has published two books on the origin of modern science.

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One Response to Pa. scientist again attacks evolution

There are three simple criticisms that demolish nearly all of Behe’s arguments. Jerry Coyne summarizes them well:

1. There is no evolutionary expectation that complex protein-protein interactions will evolve in a parasite adapting to a new drug. Any mutation that improves fitness is acceptable, regardless of what it does.
2. Behe’s probability calculations, on which his entire argument rests, are flatly wrong because they assume that adaptation cannot occur one mutation at a time. He uses chloroquine resistance of malaria (CQR) as an example, saying that the parasite always must have two mutations arising together to evolve resistance. As Ken Miller shows, this assumption is false, because one of the two mutations that Behe claims are “required” for CQR is not actually required (Chen et al. 2003, reference accidentally omitted from Miller’s piece). It is therefore bogus to take the 1/10^20 number as the estimate of the probability of the evolution of a single binding site for CQR. And it is even more bogus to use this as a generic estimate for the evolutionary probability of getting any protein-protein binding site.
3. The probability calculations are also wrong because Behe’s argument is based on specifying a priori exactly which mutations have to occur to be adaptive: the identical pair of mutations that occur in chloroquine-resistant malaria. He neglects the possibility (indeed, the certainty) that many other mutations that cause interactions between proteins and other molecules can also be adaptive.